Genetic variants in ATP6 and ND3 mitochondrial genes are not associated with aggressive prostate cancer in Mexican–Mestizo men with overweight or obesity

Mitochondrial defects have been related to obesity and prostate cancer. We investigated if Mexican–Mestizo men presenting this type of cancer, exhibited somatic mutations of ATP6 and/or ND3.Body mass index (BMI) was determined; the degree of prostate cancer aggressiveness was demarcated by the Gleason score. DNA from tumor tissue and from blood leukocytes was amplified by the polymerase chain reaction and ATP6 and ND3 were sequenced. We included 77 men: 20 had normal BMI, 38 were overweight and 19 had obesity; ages ranged from 52 to 83. After sequencing ATP6 and ND3, from DNA obtained from leukocytes and tumor tissue, we did not find any somatic mutations. All changes observed, in both genes, were polymorphisms. In ATP6 we identified, in six patients, two non-synonymous nucleotide changes and in ND3 we observed that twelve patients presented non-synonymous polymorphisms. To our knowledge, this constitutes the first report where the complete sequences of the ATP6 and ND3 have been analyzed in Mexican–Mestizo men with prostate cancer and diverse BMI. Our results differ with those reported in Caucasian populations, possibly due to ethnic differences.     

Live Your Life Out Loud

Susan Love, MD, MBA, has dedicated her professional life to the eradication of breast cancer. Author of the bestselling Dr. Susan Love's Breast Book, Dr. Susan Love's Menopause and Hormone Book, and Live a Little, Susan is Chief Visionary Officer of the Dr. Susan Love Research Foundation where she oversees an active research program centered on breast cancer cause and prevention. Susan co-founded the National Breast Cancer Coalition in the early 1990s, and she served on President Clinton's National Cancer Advisory Board from 1998–2004. Her recent projects include recruiting 377,000 women for the Love Army of Women, an Internet program that partners women and scientists to accelerate breast cancer research; and the online Health of Women Study designed to identify the cause of breast cancer. A recipient of six honorary doctorate degrees, Susan is Clinical Professor of Surgery at the David Geffen School of Medicine at the University of California, Los Angeles. In June of 2012, Susan was diagnosed with acute myelogenous leukemia and was treated with an allogenic stem cell transplant.     

An age–period–cohort analysis of cancer incidence among the oldest old,Utah 1973–2002

We used age–period–cohort (APC) analyses to describe the simultaneous effects of age, period, and cohort on cancer incidence rates in an attempt to understand the population dynamics underlying their patterns among those aged 85+. Data from the Utah Cancer Registry (UCR), the US Census, the National Center for Health Statistics (NCHS), and the National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) programme were used to generate age-specific estimates of cancer incidence at ages 65–99 from 1973 to 2002 for Utah. Our results showed increasing cancer incidence rates up to the 85–89 age group followed by declines at ages 90–99 when not confounded by the separate influences of period and cohort effects. We found significant period and cohort effects, suggesting the role of environmental mechanisms in cancer incidence trends between the ages of 85 and 100.     

Estimating development cost of an interactive website based cancer screening promotion program

ObjectivesThe aim of this study was to estimate the initial development costs for an innovative talk show format tailored intervention delivered via the interactive web, for increasing cancer screening in women 50–75 who were non-adherent to screening guidelines for colorectal cancer and/or breast cancer.MethodsThe cost of the intervention development was estimated from a societal perspective. Micro costing methods plus vendor contract costs were used to estimate cost. Staff logs were used to track personnel time. Non-personnel costs include all additional resources used to produce the intervention.ResultsDevelopment cost of the interactive web based intervention was $.39 million, of which 77% was direct cost. About 98% of the cost was incurred in personnel time cost, contract cost and overhead cost.ConclusionsThe new web-based disease prevention medium required substantial investment in health promotion and media specialist time. The development cost was primarily driven by the high level of human capital required. The cost of intervention development is important information for assessing and planning future public and private investments in web-based health promotion interventions.     

Extrapolation of Carcinogenicity Between Species: Qualitative and Quantitative Factors

Prediction of human cancer risk from the results of rodent bioassays requires two types of extrapolation: a qualitative extrapolation from short-lived rodent species to long-lived humans, and a quantitative extrapolation from near-toxic doses in the bioassay to low-level human exposures. Experimental evidence on the accuracy of prediction between closely related species tested under similar experimental conditions (rats, mice, and hamsters) indicates that: (1) if a chemical is positive in one species, it will be positive in the second species about 75% of the time; however, since about 50% of test chemicals are positive in each species, by chance alone one would expect a predictive value between species of about 50%. (2) If a chemical induces tumors in a particular target organ in one species, it will induce tumors in the same organ in the second species about 50% of the time. Similar predictive values are obtained in an analysis of prediction from humans to rats or from humans to mice for known human carcinogens. Limitations of bioassay data for use in quantitative extrapolation are discussed, including constraints on both estimates of carcinogenic potency and of the dose-response in experiments with only two doses and a control. Quantitative extrapolation should be based on an understanding of mechanisms of carcinogenesis, particularly mitogenic effects that are present at high and not low doses.     

Use of Biological Markers in Risk Assessment1

Measurements of intermediate end points in the carcinogenic process may reduce uncertainty in human risk assessment from bioassay data, by identifying sources of interspecies variation and dose nonlinearity. This paper describes desirable properties of such markers: persistence, predictive power, temporal relevance, and consistency across dose rate and species. We illustrate these properties by evaluating markers for squamous cell nasal carcinoma in rodents exposed to formaldehyde. We also discuss design issues for bioassays that evaluate markers and tumors simultaneously at necropsy.     

Cancer Fatalities from Waterborne Radon (Rn-222)

A model of the biokinetics of radon in the human body following ingestion is developed from existing data. Calculations of the probability of cancer fatality from use of radon-laden water in the home then are presented. The pathways of emanation and ingestion are examined and shown to lead to roughly equal risks. The probability of fatal cancer resulting from lifetime use of water at a radon concentration of 1 pCi/L is shown to be 1 X 10(-6), with a reasonable range between 2 X 10(-7) and 5 X 10(-6). The allowed concentration consistent with an excess risk of 10(-4) then is approximately 100 pCi/L, which is exceeded in a significant fraction of U.S. water supplies. The lifetime number of premature deaths due to waterborne radon in the U.S. is estimated to lie between 5000 and 125,000, with a best estimate of 25,000.     

Variation in Cancer Risk Estimates for Exposure to Powerline Frequency Electromagnetic Fields: A Meta-Analysis Comparing EMF Measurement Methods

We used meta-analysis to synthesize the findings from eleven case-control studies on cancer risks in humans exposed to 50-60 Hertz powerline electromagnetic fields (EMFs). Pooled estimates of risk are derived for different EMF measurement methods and types of cancer. EMF measurement methods are classified as: wiring configuration codes, distance to power distribution equipment, spot measurements of magnetic fields, and calculated indices based on distance to power distribution equipment and historic load data. Pooled odds ratios depicting the risk of cancer by each measurement type are presented for all cancers combined, leukemia for all age groups and childhood leukemia. The wire code measurement technique was associated with a significantly increased risk for all three cancer types, while spot measures consistently showed non-significant odds ratios. Distance measures and the calculated indices produced risk estimates which were significant only for leukemia.